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Spring 2015 > Block 4 neuro part 2 > Flashcards

Block 4 neuro part 2 Flashcards

1
Q

positive symptoms that can be expressed in cerebral palsy

A

hypertonia, clonus, babinski sign

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2
Q

clonus-

A

increased muscular contraction

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3
Q

negative sympotms of cerebral palsy-

A

paresis and loss of dexterity

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4
Q

spasticity-

A

velocity and direction dependent resistance to stretch in a limb

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5
Q

dystonia-

A

sustained muscle contractions causing twisting repetitive movements, abnormal postures, or both

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6
Q

most common CP is

A

spastic

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7
Q

if a baby is full term with very low birth weight and develops CP with a combo of dystonia and spasticity, what CP does he likely have?

A

spastic quadriparesis

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8
Q

if an infant had a vascular injury and developed CP, which CP does he probably have?

A

hemiparesis

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9
Q

If a premature baby develops CP, which kind does he likely have?

A

spastic diplegia

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10
Q

if a full term baby that is hypotonic at birth develops CP, what kind does he probably have?

A

dyskinetic CP

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11
Q

main goal in treatment of CP is to treat the _______

A

lack of inhibition

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12
Q

if a CP child presents with hemiplegia, what is the best treatment?

A

focal medication such as botulinum toxin

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13
Q

if a CP child has spasticity and dystonia, poor underlying strength, what kind of treatment would you give her?

A

systemic treatment, such as baclofen

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14
Q

baclofen is a _____ agonist

A

GABAb. enhances GABA function, relieving the spasticity affecting all the muscles

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15
Q

if i child has good muscle control and strength, but suffers from spasticity, they may be a good candidate for what surgery?

A

selective dorsal rhizotomy

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16
Q

if i child has good muscle control and strength, but suffers from spasticity, they may be a good candidate for what surgery?

A

selective dorsal rhizotomy

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17
Q

non associative learning-

A

behavior modification based on a single stimulus

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18
Q

sensitization-

A

increase in response to a stimulus following a novel, strong or noxious stimulus

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19
Q

how does dishabituation/sensitization work?

A

modulatory neuron releases 5HT on habituated neuron, causing cAMP synthesis –> PKA activation–> K+ channel closure–> longer depolarization–> greater Ca++ influx–> greater NT release–> greater respone

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20
Q

associative learning-

A

learning the relation between multiple stimuli

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21
Q

pre-syaptic condition relies on pairing ______ with ______

A

conditioned stimulus with unconditioned stimulus

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22
Q

Why does a conditioned stimulus need to be paired with an unconditioned stimulus to maximize response in presynaptic terminal?

A

Ca++-Calmodulin enhances adenylate cyclase, so if 5HT (US) binds without the conditioned stimulus, only some cAMP will be made, but if the CS also happens, Ca++ influx occurs and binds with Calmodulin, enhancing cAMP synthesis. With more cAMP, more PKA will be activated and more NT will subsequently be released

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23
Q

NMDA receptors need 2 things to be activated:

A

glutamate binding and depolarization of the cell (to dislodge Mg++)

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24
Q

what happens during early LTP?

A

NMDA receptors open after Mg++ is dislodged, then more AMPA receptors are inserted into postsynaptic membrane

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25
Q

what happens during late LTP?

A

Ca++ calmodulin binding activates CaCM kinase, which causes insertion of more NMDA receptors in the membrane, as well as other transcriptional modifications

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26
Q

what activates CREB?

A

cAMP

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27
Q

overall, amount of ___ entering post synaptic membrane causes LTP

A

Ca++

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28
Q

semantic memory-

A

recalling knowledge

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29
Q

______ lobe plays a critical role in declarative memory

A

medial temporal

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30
Q

______ lobe plays a critical role in declarative memory

A

medial temporal

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31
Q

encoding and retrieval of non consolidated memories occurs in ____

A

the MTL

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32
Q

consolidated memories reside in _____

A

various cortical lobes. They do not rely on the MTL

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33
Q

where are place cells located?

A

the hippocampus

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34
Q

the parts of the MTL include: (5)

A

parahippocampal cortex, perirhinal cortex, entorhinal cortex, hippocampus, and amygdala

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35
Q

describe the circuit of declarative memory in the hippocampus-

A

unimodal and polymodal association areas transmit to the perirhinal and parahippocampal cortices–> entorhinal cortex–> hippocampus

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36
Q

olfaction feeds directly into the _____ cortex

A

entorhinal

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37
Q

what serves as the gateway into the hippocampal formation?

A

entorhinal cortex

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38
Q

The _____ integrates information and rapidly fuses these features into a coherent memory trace retained in the cortex

A

hippocampus

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39
Q

left pre-frontal cortex allows for “_____” responses

A

remember

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40
Q

the right prefrontal cortex allows for “_____” responses

A

Know

i.e. “I know X is true”

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41
Q

what 2 regions are involved retrieval of old episodic memories but are usually deactivated during episodic encoding?

A

posterior lateral parietal and posterior midline regions

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42
Q

priming-

A

change in the processing of a stimulus due to a previous encounter with the same or a related stimulus, in the absence of conscious awareness of the original encounter

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43
Q

______ cortex shows less activity in the related-word than unrelated-word condition. So its involved in distinguishing unrelated words

A

anterior temporal cortex

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44
Q

Causes of Alzheimer’s disease include mutation in which 3 genes?

A

gene producing amyloid precursor protein (APP), proteins that process APP, and ApoE gene

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45
Q

4 abnormalities are observed in the brain of someone who died from AD:

A

neurofibrillary tangles, amyloid plaques, loss of neurons, and loss of synaptic contact

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46
Q

vascular disease of the MTL shows significant loss of ____ neurons

A

CA1

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47
Q

what 3 things are most heavily affected by AD and which 2 are relatively spared?

A
  • entorhinal cortex (mostly layer 2), CA1 neurons, and subiculum
  • dentate gyrus and CA3 neurons
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48
Q

TLE =

A

temporal lobe epilepsy

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49
Q

TLE affects what layer of the entorhinal cortex?

A

Layer 3

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50
Q

TLE destroys ____ and ___ neurons, as well as the _____ gyrus.

A

CA1, CA3, dentate

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51
Q

big difference between AD and TLE?

A

AD affects layer 2 of entorhinal cortex, TLE affects layer 3

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52
Q

what is the best way to keep a healthy hippocampus?

A

keep exercising it!

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53
Q

How do we know NMDA involved in fear conditioning?

A

if you block NMDA receptors in the amygdala with CPP, the animal will not learn a fear response to a stimulus.

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54
Q

stress enhances fear memory via

A

glucocorticoids

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55
Q

stress enhances fear memory consolidation via

A

glucocorticoids

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56
Q

Korsakoff Sydrome is due to damage to the-

A

DM nucleus of the thalamus, mammillary bodies, and disrupted circuitry to anterior cingulate gyrus

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57
Q

Symptoms of Korsakoff Syndrome

A

retrograde memory problems, psychiatric symptoms including apathy and story fabrication, anterograde amneisa

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58
Q

Who often gets Korsakoff Syndrome?

A

chronic alchoholics with vitamin B1 deficiency

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59
Q

Who often gets Korsakoff Syndrome?

A

chronic alchoholics with vitamin B1 deficiency

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60
Q

3 genes identified as being linked to AD

A

APP, PS-1, PS-2

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61
Q

what stage of AD do people begin to notice symptoms?

A

3

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62
Q

how do tangles contribute to AD?

A

they collapse and twist to destroy vital cell transport systems

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63
Q

how do beta amyloid plaques contribute to AD?

A

they clump together and block synapses, as well as trigger inflammation

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64
Q

What are the earliest clinical signs of AD?

A

olfactory loss, short term memory loss, and loss of place cells

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65
Q

Cleavage of the APP by _________ leads to formation of Abeta fragments that lead to plaques

A

beta and gamma secretase

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66
Q

cleavage of APP by ______ prevents the formation of Abeta fragments

A

alpha secretase

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67
Q

polymorphisms in the ____ gene are a prominent risk factor for AD

A

ApoE

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68
Q

inheritance of the ApoE4 gene _____ risk of AD, inheritance of the ApoE2 gene ______ risk of AD

A
  • increases

- decreases

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69
Q

AD pathophysiology: when APP is cleaved by beta or gamma secretase, it leads to the formation of ______, which aggregates into plaques

A

Abeta42

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70
Q

Formation of Abeta plaques alone isn’t enough to cause AD. Plaque formation must be coupled with an inability to _______, for disease to occur

A

remove the plaques

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71
Q

Stage 3 AD symptoms can be summarized as:

A

cognitive problems of a wide variety that have begun to be noticed

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72
Q

Stage 4 AD symptom summary:

A

begin having difficulty with tasks, forgetfulness about one’s own history, moody in social situations

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73
Q

Stage 5 AD symptom summary:

A

begin needing help with day to day activities, confusion

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74
Q

Stage 6 AD symptom summary:

A

very bad memory, change in sleep patterns, need help with bathroom, major personality changes

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75
Q

Stage 7 AD symptom summary:

A

begin to stop responding to environment and moving. May still say words

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76
Q

Where else can you find Abeta plaques?

A

Drusen, in age related macular degeneration

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77
Q

______ is reduced in the CA1 region of the AD brain

A

Neuroprotectin D1 (NPD1)

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78
Q

people with AD have a decreased ability to make what protective protein?

A

NPD1

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79
Q

What substance can hold back inflammation and protein misfolding in the brain, as well as help in nerve regeneration and induce neuroprotection?

A

DHA

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80
Q

DHA attenuates _____ secretion and enhances ______ biosynthesis

A
  • Abeta

- NPD1

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81
Q

DHA attenuates _____ secretion and enhances ______ biosynthesis

A
  • Abeta

- NPD1

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82
Q

NPD1 shifts APP processing from ______ pathway to _____ pathway

A

amyloidogenic to non-amyloidogenic

83
Q

B94 is associated with ______

A

inflammation

84
Q

NPD1 reduced what pro-inflammatory compounds in brain?

A

COX-2 and B94

85
Q

what does PPAR gamma do?

A

blocks beta-secretase activity

86
Q

neurofibrillary tangles actually accumulate in a confined manner in limbic regions including _______ and ______ as part of normal aging.

A
  • entorhinal cortex

- hippocampal CA1

87
Q

the initial trigger of AD is:

A

Abeta aggregation

88
Q

Decreases in CSF ____ are the first hallmark of AD and precede an in increase in CSF tau.

A

Abeta42

89
Q

why does a decrease in Abeta42 indicate AD?

A

brain is not removing this protein fragment well enough anymore

90
Q

if tau NF tangles are a normal process, what induces them to be pathogenic?

A

Abeta

91
Q

if tau NF tangles are a normal process, what induces them to be pathogenic?

A

Abeta

92
Q

why does CNS regrowth fail?

A

inhibitory signals from glial cells and crowding from glial cells responding to immune system mediated clearance of damaged tissue

93
Q

order of nerve death:

A

nerve terminal degenerates–> distal terminal separates and degenerates–> myelin fragments–> phagocytic cells invade–> cell body swells and nucleus gets eccentric–> presynaptic terminal (dendrites of damaged nerve) retracts–> glial cells invade presynaptic terminal

94
Q

_______ cells mediate peripheral nerve growth through secretion of signals to promote growth cone

A

schwann cells

95
Q

schwann cells secrete _____, ____, _____ into ECM. These are the “bread crumbs”

A

laminin, fibronectin, and collagens

96
Q

the inflammatory response to CNS nerve destruction attracts ______, which inhibit neural growth

A

astrocytes

97
Q

______ factors promote axon regeneration by activating _____ receptors

A
  • ciliary neurotrophic (CNTF)

- GP130

98
Q

_____ inhibits regrowth by blocking the GP130 receptors

A

SOCS3

99
Q

the difference between a cut and crushed nerve regeneration:

A

cut nerves have to clear debris and use a growth cone to REGROW the nerve, whereas crushed nerves are REPAIRED by schwann cells secreting NGF

100
Q

when a peripheral nerve is cut, which cell expresses growth related genes and which cell releases ECM molecules to guide regeneration?

A
  • damaged neuron expresses growth genes

- schwann cells

101
Q

when a peripheral nerve is cut, which cell expresses growth related genes and which cell releases ECM molecules to guide regeneration?

A
  • damaged neuron expresses growth genes

- schwann cells

102
Q

what 2 factors guide axons back to their target NMJ’s?

A

NGF and BDNF

103
Q

what is the necessary to reestablish a NMJ after peripheral nerve damage?

A

the original synapse must be maintained and the muscle health and anatomy must be maintained

104
Q

to reinnervate the same NMJ after nerve destruction, the synapse must maintain 2 things:

A

synaptic specialization and AChR receptor clustering

105
Q

this factor promotes/maintains AChR clustering

A

agrin

106
Q

this transmembrane protein version of tyrosine kinase functions as an agrin receptor critical to AChR clustering

A

MuSK

107
Q

responsible for transcription of AChR at post-synaptic site

A

Neurogulin-1

108
Q

AChR’s in damaged muscle should ______ and ______ so that the growing axon can find them

A

cluster and proliferate

109
Q

do nerves have specificity for their regrowth target?

A

absolutely. In an experiment where C8 and T5 ganglion were transplanted then the subsequently grew to synapse on nerves of their original level. So take a C8 ganglion and put it in the superior cervical ganglion, its axons will grow towards C8 targets

110
Q

3 main reasons CNS doesnt grow back like peripheral

A
  1. Central damage initiates programmed cell death
  2. CNS doesn’t secrete ECM scaffolding to guide axons
  3. CNS secretes inhibitory factors (chemorepellants)
111
Q

Glial scars inhibit axon regrowth by secreting _____

A

OLIG-2

112
Q

why does a stroke cause neuron death?

A

hypoxia leads to a halt in ATP production, which means it can no longer maintain electrochemical gradient and depolarizes. The depolarization causes excitotoxicity, leading to oxidative stress/necrosis. Additionally, all the glutamate spills out of this dead neuron and causes peri-infarct depolarization in neighboring neurons–> calcium overload–> mitochondrial damage–> apoptosis

113
Q

penumbra-

A

region where neurons are injured but not dead

114
Q

penumbra can be limited by neuroprotective factors such as ____

A

NPD-1

115
Q

2 factors that block apoptosis-

A

NGF and Bcl-2

116
Q

cytokines released in inflammatory response to nerve damage block the anti-apoptosis effect of ____

A

Bcl-2

117
Q

____ is implicated in cancer, as it blocks apoptosis

A

Bcl-2

118
Q

ATP is depleted in necrosis or apoptosis?

A

necrosis

119
Q

which is irreversible, apoptosis or necrosis?

A

necrosis

120
Q

the degree of postnatal neurogenesis decreases with increasing _________

A

brain complexity

121
Q

mammals show postnatal neurogenesis in what 2 areas?

A

subgranular zone of the hippocampal dentate gyrus and the subventricular zone

122
Q

subventricular zone contributes interneurons to

A

the olfactory bulb

123
Q

interneurons generated in adult neurogenesis are carried to their targest by

A

the rostral migratory stream RMS

124
Q

interneurons generated in adult neurogenesis are carried to their targest by

A

the rostral migratory stream RMS

125
Q

what cells act as stem cells in the SVZ (subventricular zone)

A

astrocytes

126
Q

the best way to augment brain development is ______, not drugs or implants

A

lifestyle changes

127
Q

the major regulator of hippocampal neurogenesis is

A

hippocampus dependent learning

128
Q

what can block environmentally induced neurogenesis of the hippocampus?

A

opioid pain killing drugs

129
Q

rubrospinal tract sends excitatory signals to _____ in the upper extremity

A

flexors

130
Q

which tract is responsible for decorticate posturing?

A

rubrospinal tract

131
Q

medial vestibulospinal tract is responsible for

A

head-neck movement

132
Q

lateral vestibulospinal tract is responsible for

A

proximal estensors for posture and balance

133
Q

which tract is responsible for decerebrate posturing?

A

reticulospinal tract

134
Q

_____ tract resonsible for head and eye movements

A

tectospinal

135
Q

UMN lesion of CN VII =

A

flaccid paralysis on lower contra face

136
Q

LMN lesion of CN VII =

A

bells palsy

137
Q

CN X UMN lesion =

A

uvula deviates to same side as lesion

138
Q

CN X LMN lesion =

A

uvula deviates to opposite side of lesion

139
Q

CN XII UMN lesion =

A

tongue deviates to opposite side of lesion

140
Q

CN XII LMN lesion =

A

tongue deviates to same side of lesion

141
Q

CN XII LMN lesion =

A

tongue deviates to same side of lesion

142
Q

pain and temperature sensory neurons terminate on cell bodies in ___________ in the dorsal horn, then secondary neurons decussate and terminate in the _____.

A
  • rexed laminae I, II, and V

- VPL

143
Q

spinal trigeminal nucleus conveys

A

pain and temperature

144
Q

principle sensory nucleus conveys

A

two point touch and vibration

145
Q

mesencephalic nucleus conveys

A

proprioception

146
Q

motor nuclei are medial to the

A

sulcus limitans

147
Q

motor nuclei are medial to the

A

sulcus limitans

148
Q

CN VII contributes to what 3 nuclei?

A

superior salivatory, facial, and solitary

149
Q

CN VII contribution to superior salivatory nucleus is:

A

GVE, parasympathetic to lacrimal, submandibular, and sublingual gland

150
Q

CN VII contribution to the facial nucleus is:

A

SVE, muscles of facial expression

151
Q

CN VII contribution to the solitary nucleus (rostral portion) is:

A

SVA, taste

152
Q

CN IX contributes to what 3 nuclei?

A

solitary, ambiguus, and salivatory

153
Q

CN IX contribution to the rostral part of the solitary nucleus is:

A

SVA, taste

154
Q

CN IX contribution to the caudal part of the solitary nucleus is:

A

GVA, sensory info from pharynx

155
Q

CN IX contribution to the nucleus ambiguus is:

A

SVE, pharynx and larynx musculature (very small component)

156
Q

CN IX contribution to the inferior salivatory nucleus is:

A

GVE, parasympathetic to the parotid gland

157
Q

CN X contributes to what 3 nuclei?

A

solitary, ambiguus, and dorsal motor

158
Q

CN X contribution to the rostral solitary nucleus is:

A

SVA, taste

159
Q

CN X contribution to the caudal solitary nucleus is:

A

GVA, cardiorespiratory and digestive sensory info

160
Q

CN X contribution to the nucleus ambiguus is:

A

SVE, pharynx and larynx musculature

161
Q

CN X contribution to the dorsal motor nucleus is:

A

GVE, parasympathetics to cardiovascular and digestive systems

162
Q

What is the only LMN that shows contralateral signs?

A

CN IV

163
Q

Inferior alternating hemiplegia occurs at what level and affects what nucleus?

A

medulla, CN XII

164
Q

middle alternating hemiplegia occurs at what level and affects what nerve?

A

pons, CN VII

165
Q

superior alternating hemiplegia occurs at what level and affects what nerve?

A

midbrain, CN III

166
Q

PICA lesion leads to ______ syndrome

A

wallenberg

167
Q

what arteries supply the medulla?

A

ASA, PICA, and paramedian branches of vertebral

168
Q

what 4 arteries supply the pons?

A

paramedian branches of basilar artery, short and long circumferential branches of the basilar artery, and AICA

169
Q

4 arteries supplying midbrain:

A

PCA, SCA, quadrigeminal artery

170
Q

4 arteries supplying midbrain:

A

PCA, SCA, quadrigeminal artery

171
Q

_______ effects the pyramidal tract, medial lemniscus, hypoglossal nucleus. Produced by block of paramedian branches of and anterior spinal arteries

A

Medial medullary syndrome

172
Q

___________ effects the inf. cerebellar peduncle, vestibular nu, sp. trigeminal nu., anterolateral system, nucleus ambiguus, nu. solitarius, descending sympathetic fibers. Produced by block of PICA and/or Vertebral A.

A

PICA/Wallenberg sydrome

173
Q

__________ effects corticospinal and corticobulbar tracts, facial colliculus (also abducens nu, medial lemniscus). Produced by block of paramedian branches of basilar artery, ventral and dorsal territories.

A

Foville’s syndrome

174
Q

________ effects middle cerebellar peduncle, vestibular nu, trigeminal nu., anterolateral system, cochlear nuclei, descending sympathetic fibers

A

AICA syndrome

175
Q

_________ affects oculomotor nerve or fascicles produced by block of branches of PCA and top of the basilar artery.

A

Weber’s syndrome

176
Q

_________ affects oculomotor nerve, red nucleus, and sup. cerebellar penduncle. Produced by block of branches of PCA and top of the basilar artery

A

Claude’s syndrome

177
Q

_______ affects same as above plus substantia nigra, cerebral peduncle. Same arteries blocked.

A

Benedikt’s syndrome

178
Q

Pt presents with aggression, refusal to eat, and no fear. Diagnosis?

A

bilateral loss of amygdala

179
Q

Pt presents with pre-existing mental disorder, impairment of consciousness, and short term memory loss. Diagnosis?

A

unilateral hippocamal infarction

180
Q

Pt. presents with behavior change, episode of impairment of consciousness, and progressive mental disorder (depression and psychosis)
Diagnosis?

A

paraneoplastic limbic encephalitis

181
Q

Pt. presents with flu-like illness, seixures, and multiple anti-seizure drugs were unable to stop the seizures (meaning she had status epilepticus) Diagnosis?

A

limbic encephalitis with prefrontal involvement. She may have also had short term memory deficits from this

182
Q

Pt presents with impaired consciousness, dream state, deja vu, picking at clothing, olfactory hallucinations. Diagnosis?

A

Limbic seizure

183
Q

Pt. presents with acute episode of disorientation and memory difficulties, history of cocaine use, and short term memory deficit. Diagnosis?

A

Cocaine-induced hippocampi infarction

184
Q

Pt. is being rehabbed for Acomm aneurysm and has motor deficits and memory impairment (global, short term, verbal, visual) Diagnosis?

A

Ischemia in Fornix (the mustache of the brain) and premotor involvement.

185
Q

Pt. presents with confusion, short term memory loss, ocular dysfunction, gait ataxia, dysarthria, paresthesias of legs. Diagnosis?

A

Wernicke’s Encephalopathy

186
Q

Pt. presents with anterograde and retrograde amnesia, confabulation, lack of insight, apathy. Diagnosis?

A

Korsakoff’s syndrome

187
Q

Pt. presents with anterograde and retrograde amnesia, confabulation, lack of insight, apathy. Diagnosis?

A

Korsakoff’s syndrome

188
Q

Pt. presents with anterograde and retrograde amnesia, confabulation, lack of insight, apathy. Diagnosis?

A

Korsakoff’s syndrome

189
Q

Echolalia-

A

tendency to mimic what you hear from others. Using phrases from TV instead of independently carrying conversation

190
Q

autistic children show insistence on sameness =

A

intensity on a specific object or theme at high, unusal intensity

191
Q

how many children have some form of ASD?

A

1/68

192
Q

M/F ratio of autism diagnosis

A

4-5 males per female

193
Q

Neuroimaging findings of autistic children found they have above average ______ and below average number of ______ cells in the cerebellum

A
  • head circumference

- purkinje

194
Q

often a diagnosis of ASD comes from both an absence of _____ and a presence of ______

A

typical behaviors

atypical behaviors

195
Q

Level 1 assesment for ASD does what?

A

identifies children at risk for ASD and passes them on to level 2

196
Q

level 2 assesment for ASD does what?

A

determines if child meets criteria for diagnosis of ASD

197
Q

Early signs of ASD include abnormalities in 3 things:

A

joint attention (moving attn. btw object and adult to share appreciation for the object), social interaction, and play

198
Q

should a child that does not how signs of autism be screened for it anyways?

A

yes, you do not want to “wait and see”

199
Q

Absolute indicators for immediate further evaluation for autism include no ____ at 12 months, no _____ at 16 months, and no ______ at 24 months

A
  • babbling or gesturing
  • single words
  • two word spontaneous phrases
200
Q

3 screenings done in level 1 autism assesment:

A

MCHAT, pervasive developmental disorders screening test 2, social communication questionnaire

201
Q

2 tests done in a level 2 autism assesment

A

ADI-R (autism diagnostic interview) and autism diagnostic observation schedule (ADOS-2)

202
Q

process of applying interventions based on principles of learning derived from experimental psychology to systematically change behavior-

A

Applied Behavioral Analysis (ABA)

203
Q

ABA is used to generalize __________

A

behaviors to new environments or situations

Spring 2015 (9 decks)

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